Abstract

Patients with chronic heart failure (CHF) experience significant morbidity because of dyspnea and fatigue with activities of daily living. Although central hemodynamic abnormalities are the hallmark of this disorder, investigators have not shown a relationship between left ventricular ejection fraction or exercise pulmonary capillary wedge pressure and exercise intolerance in this disorder. Recent studies have focused on the contributions of pulmonary abnormalities and alterations in peripheral vasomotor control and skeletal muscle in exercise intolerance in this disorder. Early anaerobic metabolism occurs in patients with CHF and appears to be caused by a combination of reduced skeletal muscle blood flow and decreased aerobic enzyme content in skeletal muscle. Atrophy in skeletal muscle and alterations in skeletal muscle fiber typing are accompanied by alterations in contractile function in skeletal muscle. These results suggest that exercise intolerance in patients with CHF is multifactorial, and that research efforts must consider central hemodynamic abnormalities, pulmonary abnormalities, and alterations in peripheral blood flow and skeletal muscle biochemistry and histology. The present review will explore current research in this area and develop a model for understanding exercise intolerance in CHF.

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